慢性乙肝患者外周血单个核细胞中CXCR1、CXCR2及IL-8 mRNA表达与干扰素治疗关系

目的:了解乙型肝炎病毒(HBV)慢性感染患者外周血单个核细胞(PBMC)中CXCR1、CXCR2及IL-8 mRNA表达水平及与α干扰素(IFN-α)治疗的关系。方法:采用实时定量PCR法动态观察30例慢性乙型肝炎患者接受IFN-α治疗前、治疗3个月、6个月后其外周血单个核细胞CXCR1、CXCR2及IL-8 mRNA表达水平。结果:治疗前慢性乙肝患者CXCR1、CXCR2及IL-8 mRNA表达水平分别为(0.44740.0386)、(0.4720 0.0458)、(1.1897 0.1028),均高于正常对照组(n=36),其中CXCR1及IL-8 mRNA水平升高显著,差异有统计学意义(P<0.01)。治疗过程中CXCR1、CXCR2及IL-8表达水平均显著下降。IFN-α治疗6个月后CXCR1、CXCR2及IL-8 mRNA表达水平分别为(0.41290.0395)、(0.4461 0.0477)、(0.8660 0.1307),与治疗前相比,差异有显著性(P<0.01或P<0.05)。治疗前的CX-CR1、CXCR2及IL-8的表达水平在HBV高复制组(HBV-DNA>106,n=22)明显高于HBV低复制组(HBV-DNA<106,n=8),差异有统计学意义(P<0.05)。结论:慢性乙肝患者外周血单个核细胞中CXCR1和IL-8表达水平显著升高,在干扰素治疗后,其表达水平下调,证明其可能与慢性乙肝炎症的发生机制相关。     

CXCL8及其受体CXCR1、CXCR2在慢性乙肝患者外周血PMNs中的表达

目的:探讨慢性乙肝患者外周血中性粒细胞(PMNs)上CXCL8及其受体CXCR1、CXCR2的表达。方法:以中性粒细胞分离液分离、纯化PMNs,检测患者血清HBe Ag及PMNs内HBV DNA,入选患者依据检测结果进行分组,SABC免疫细胞化学染色法检测各组患者PMNs内CXCL8及其受体CXCR1、CXCR2的表达。结果:SABC免疫细胞化学染色结果显示,CXCL8主要位于PMNs胞浆中,CXCR1、CXCR2多见于胞浆和胞膜上。其中HBe Ag(+)者CXCL8、CXCR1免疫着色较深,而CXCR2免疫着色较浅;PMNs内HBV DNA(+)者CXCL8、CXCR1免疫着色亦较深,而CXCR2免疫着色亦较浅。患者CXCL8和CXCR1的水平均显著升高,与正常对照相比,差异均有显著性(P0.05),而CXCR2的表达无统计学意义(P0.05)。结论:HBV侵染中性粒细胞后可促进CXCL8分泌,使胞膜CXCR1表达进一步增强。CXCL8、CXCR1、CXCR2免疫组化染色程度与患者HBe Ag表达、HBV DNA载量密切相关。高表达CXCR1的中性粒细胞与CXCL8相互作用,趋化吸引更多PMNs至病灶,参与局部炎性损伤和组织修复。     

趋化因子CXCL12及其配体CXCR4、CXCR7对HER2阳性乳腺癌细胞生物学功能的影响北大核心CSCD

目的:探究趋化因子CXCL12及其配体CXCR4、CXCR7对HER2阳性乳腺癌细胞增殖、细胞周期、迁移、侵袭和上皮-间质转化(EMT)的影响。方法:体外培养HER2阳性乳腺癌细胞BT474,应用siRNA转染技术单独或联合沉默CXCR4、CXCR7,RT-PCR与Western blot检测转染效率;应用CXCL12刺激上述转染细胞,并将其分为5组,A组:正常培养的BT474细胞;B组:CXCL12处理的BT474细胞;C组:CXCL12处理的转染si-CXCR4细胞;D组:CXCL12处理的转染si-CXCR7细胞;E组:CXCL12处理的联合转染si-CXCR4与si-CXCR7细胞;应用CCK-8、流式细胞术、划痕实验、侵袭实验及Western blot分别检测沉默CXCR4和(或)CXCR7对CXCL12诱导的乳腺癌细胞增殖、细胞周期进展、迁移、侵袭和EMT行为的影响。结果:转染siRNA能显著降低BT474细胞中CXCR4和(或)CXCR7的mRNA和蛋白表达水平(P<0.01);单独或联合沉默CXCR4与CXCR7均能明显抑制CXCL12对乳腺癌细胞增殖、细胞周期进展、迁移、侵袭行为的促进作用(P<0.05或P<0.01),并以联合沉默CXCR4与CXCR7时效果最为显著(P<0.01),与单独沉默CXCR7相比,沉默CXCR4更能抑制CXCL12对乳腺癌EMT的促进(P<0.05)。结论:沉默CXCR4或CXCR7表达均能抑制CXCL12对HER2阳性乳腺癌细胞增殖、细胞周期进展、迁移、侵袭的促进功能,但CXCL12主要通过与CXCR4相互作用来促进乳腺癌的EMT行为,而同时抑制CXCR4或CXCR7能更有效地抑制CXCL12的上述功能。     

胃癌组织中CXCL12和CXCR4的表达及意义

目的观察趋化因子CXCL12及其特异性受体CXCR4在人胃癌组织中的表达,探讨其与临床病理参数、预后的关系。方法选择120例胃癌标本,应用免疫组化SP法检测CXCL12和CXCR4在人胃癌组织中的表达,分析CXCL12和CXCR4的表达与患者临床病理参数、术后生存率之间的关系。结果胃癌组织及正常胃黏膜组织中均可检测到CXCL12、CXCR4的表达,但胃癌组织中的表达水平均明显高于正常胃黏膜组织,表达差异有显著性(P<0.05)。CXCL12阳性与CXCR4阳性呈正相关(r=0.276,P<0.05)。胃癌CXCL12和CXCR4的表达水平与肿瘤细胞淋巴结转移及分化程度密切相关(P<0.05),与患者的年龄、性别、肿瘤的大小、浸润深度及远处转移等无关(P>0.05)。CXCL12和CXCR4阳性表达的患者其五年生存率明显低于其阴性表达的患者。结论胃癌中CXCL12和CXCR4的高表达与胃癌的生物学行为及预后密切相关,检测其表达对预测胃癌的转移及判断预后有一定价值。     

经腹超声引导下清宫术治疗对子宫瘢痕妊娠患者受体CXCR1和CXCR2 mRNA表达的影响

目的 探讨经腹超声引导下清宫术治疗对子宫瘢痕妊娠(cesarean scar pregnancy, CSP)患者受体CXCR1和CXCR2 mRNA表达的影响。方法 前瞻性收集2019年6月至2021年1月上海市松江区妇幼保健院收治的CSP患者96例患者为CSP组,并选取同期的入本院接受剖宫产手术的正常妊娠患者90例为正常妊娠组。实时荧光定量PCR检测血清或组织中IL-8及受体CXCR1和CXCR2 mRNA的水平。免疫组化法检测IL-8及受体CXCR1和CXCR2的阳性表达。结果 与正常妊娠组相比,CSP组中子宫内膜组织和血清中IL-8及受体CXCR1和CXCR2 mRNA的表达水平显著升高(P<0.05);清宫术前和术后24h对比,血清中IL-8及受体CXCR1和CXCR2 mRNA水平对比差异无统计学意义(P>0.05),与清宫术前和术后24h对比,术后30d血清中IL-8及受体CXCR1和CXCR2 mRNA水平显著降低(P<0.05);复发的患者中血清中IL-8及受体CXCR1和CXCR2 mRNA水平的表达明显高于未复发的患者(P<0.05);复发组...     

外周血CD4+CXCR5+滤泡辅助性T细胞与慢性乙型肝炎患者高球蛋白血症相关

目的 检测外周血CD4+ CXCR5+滤泡辅助性T细胞(Tfh细胞)的频率及其表面标志,分析与慢性乙型肝炎(乙肝)患者高球蛋白血症的关系.方法 收集健康人、乙肝患者及乙肝高球蛋白血症患者的外周血,分离血浆及外周血单个核细胞(PBMC),ELISA检测血浆中IL-21、CXCL13和IFN-γ水平,流式细胞术检测PBMC中CD4+ CXCR5+ Tfh细胞的频率及其表面PD-1、ICOS及CD40L的表达情况.结果 乙肝高球蛋白血症患者外周血CD4+ CXCR5+ Tfh细胞占CD4+T细胞的百分比(22.6±4.7)％明显高于普通慢性乙肝患者(11.9±3.9)％及健康志愿者(6.8±3.9)％,CD4+ CXCR5+ Tfh细胞上PD-1和CD40L的表达水平升高,血清IL-21及CXCL13水平升高,而IFN-γ水平降低,差异具有统计学意义(P＜0.05).结论 外周血CD4+ CX-CR5+ Tfh细胞与乙肝高球蛋白血症的发病相关.     

职业性三氯乙烯药疹样皮炎CXCR2和CXCR3基因的表达

目的: 建立荧光定量PCR检测三氯乙烯药疹样皮炎(DMLT)患者外周血淋巴细胞CXCR2和CXCR3 mRNA表达的方法.方法: 利用SYBR Green荧光定量PCR分别检测24例DMLT患者、 26例正常人外周血淋巴细胞CXCR2和CXCR3基因mRNA表达情况,以β2微球蛋白基因作为内参,根据相对定量公式 (2-△△CT)计算DMLT患者与正常人CXCR2和CXCR3基因表达差异倍数.结果: 24例患者外周血淋巴细胞荧光定量PCR均检出CXCR2和CXCR3 mRNA表达,其中CXCR2表达情况有两种: 表达上升14例(58.3%)和表达下降10例(41.7%),与正常人CXCR2 mRNA相比表达倍数分别为16.76±7.01、 0.54±0.30;CXCR3表达显著升高(△CT=6.3±2.8,11.4±1.9;P<0.01),与正常人CXCR3 mRNA相比表达倍数为33.37±31.61.结论: 成功建立了DMLT患者外周血淋巴细胞CXCR2和CXCR3mRNA表达的荧光定量PCR方法.     

CXCL12、CXCR4、MMP-2在宫颈鳞癌组织的表达及意义

目的探讨趋化因子CXCL12与其受体CXCR4及金属蛋白酶MMP-2在宫颈鳞癌组织中的表达及临床意义。方法采用免疫组织化学SP法检测50例宫颈鳞癌组织及50例癌旁正常组织中CXCL12、CXCR4、MMP-2的表达。结果 CXCL12、CXCR4、MMP-2在宫颈鳞癌组织中的阳性表达率(68.0%、72.0%、78.0%)明显高于正常宫颈组织(12.0%、24.0%、30.0%),在中/低度分化的宫颈鳞癌组织阳性表达率分别为84.4%、75.0%、87.5%。CXCL12、CXCR4、MMP-2在宫颈鳞癌淋巴结转移组中阳性表达率(86.2%、82.8%、79.3%)也明显高于无淋巴结转移组(52.4%、57.1%、52.4%)。在宫颈鳞癌组织中CXCL12与CXCR4、MMP-2表达都呈正相关(r=0.355,P=0.004;r=0.310,P=0.036);MMP-2与CXCR4表达也呈正相关(r=0.297,P=0.042)。结论 CXCL12和受体CXCR4、MMP-2与宫颈鳞癌的病变进展和转移密切相关,可能对宫颈鳞癌的预后和复发具有指导意义。     

循环纤维细胞通过CXCR4介导的趋化作用参与类风湿性关节炎发病

目的探索循环纤维细胞(CF)在类风湿性关节炎(RA)中的作用及其与CXC趋化因子配体12-CXC趋化因子受体4(CXCL12-CXCR4)的关系。方法收集77例RA患者外周血及部分患者的滑液和21例健康对照的外周血样本,采用流式细胞术检测CF在外周血及滑液中的比例及其表面CXCR4水平,并分析其与28个关节疾病活动度评分(DAS28)的相关性;ELISA检测血清及滑液中CXCL12水平,通过Transwell~(TM)实验检测CXCL12对表达CXCR4+CF的趋化能力,应用CXCR4拮抗剂普乐沙福(plerixafor/AMD3100)观察对趋化作用的影响。结果与正常对照组相比,RA患者外周血中CF比例显著增加,其比例与DAS28评分呈正相关;RA患者滑液中CF比例及其表面CXCR4表达均高于外周血;滑液中CXCL12表达水平及对CF的趋化能力均高于外周血;在滑液及外周血中细胞经CXCR4抑制剂AMD3100处理后,CF趋化显著减少。结论 CF可通过由CXCR4介导的趋化作用参与RA的发病。     

大肠癌中SDF-1与CXCR4的表达及临床意义

目的观察基质细胞衍生因子1(stromal cell-derived factor 1,SDF-1)及其受体CXCR4蛋白和mRNA在大肠腺癌、大肠管状腺瘤、非肿瘤性大肠黏膜组织中的表达,探讨二者在大肠腺癌的发生、发展、浸润转移中的作用。方法采用免疫组化SP两步法和RT-PCR法检测上述3组中SDF-1和CXCR4蛋白、mRNA的表达。结果 (1)免疫组化SP两步法检测SDF-1、CX-CR4的蛋白在非肿瘤性大肠黏膜、大肠管状腺瘤、大肠腺癌中的阳性表达量呈明显递增,组间差异均有统计学意义(P<0.05);(2)RT-PCR检测SDF-1和CXCR4的mRNA在大肠腺癌组中的表达高于非肿瘤性大肠黏膜组(P<0.01);(3)大肠腺癌组SDF-1、CXCR4的蛋白与mRNA的表达均与癌组织的浸润深度、淋巴结转移有关(P<0.05,P<0.01);(4)大肠腺癌组织中SDF-1和CXCR4二者间的蛋白、mRNA表达均呈正相关(r=0.436,P<0.01;r=0.949,P<0.01)。结论 SDF-1和CXCR4在大肠腺癌组织中高表达,可能与大肠腺癌的发生、浸润、转移密切相关。     

Constitutive expression of growth regulated oncogene (gro) in human colon carcinoma cells with different metastatic potential and its role in regulating their metastatic phenotype

The purpose of this study was to examine the expression and functional significance of the growth-regulated oncogene (gro) family in human colon carcinoma growth and metastasis. We examined constitutive expression of CXCL1 (gro-alpha), CXCL2 (gro-beta), CXCL3 (gro-gamma) and their receptor, CXCR2 in human colon carcinoma cells with different metastatic potentials. Non-metastatic and low metastatic cells expressed lower levels of CXCL1 and CXCR2 mRNA and protein as compared to high metastatic colon carcinoma cells. No difference in CXCL2 and CXCL3 mRNA expression levels was observed. Colon carcinoma cells expressing higher levels of CXCL1 exhibit increased proliferation and invasive potential. Furthermore, exogenous addition of recombinant human CXCL1 significantly enhanced the proliferation and invasiveness of colon carcinoma cells. Furthermore, treatment of KM12C cells with exogenous CXCL1 enhanced their invasiveness. Neutralizing antibody to CXCL1 in combination with antibody to CXCR2 inhibited highly metastatic KM12L4 (high CXCL1 expressor) cell proliferation. These data demonstrate that the constitutive expression of CXCL1 and its receptor CXCR2 is associated with metastatic potential and modulates colon cancer cell proliferation and an invasive phenotype.     

肺炎支原体肺炎患儿外周血CXCL8 及其mRNA 表达

目的:探讨支原体肺炎患儿外周血CXCL8 及其mRNA 表达的临床意义。方法:收集2013 年10 月~2015 年3 月淮南市妇幼保健院收治的支原体肺炎患儿48 例,其中重症12 例,轻症36 例,以ELISA 法检测患儿血清CXCL8 含量,PCR法检测患儿外周血单个核细胞内CXCL8 mRNA 水平。以GAPDH 为参照,以lgcDNA/ lgGAPDH 比值代表其最终mRNA 水平。结果:支原体肺炎患儿外周血血清CXCL8 含量及外周血单个核细胞内CXCL8 mRNA 水平分别为(298.917±51.860)pg/ ml、(1.848±0.525)lgcDNA/ lgGAPDH,与正常对照相比差异均有显著统计学意义(P<0.05)。进一步观察发现,重症患儿外周血CXCL8 及其mRNA 进一步升高,与轻症组相比,血清CXCL8 含量差异无显著统计学意义统计学意义(P>0.05),而CXCL8mRNA 水平差异有显著统计学意义(P<0.05)。急性期以红霉素静脉注射7 ~10 d,使患儿病情得以明显控制,咳嗽症状减轻,肺部炎症逐渐改善,病情得到有效控制,再以阿奇霉素序贯治疗2 ~3 周,患儿病情逐步由急性期转为恢复期,此时患儿外周血CXCL8 及其mRNA 水平明显降低,与急性期相比,差异有显著统计学意义(P<0.05)。结论:支原体肺炎患儿外周血CXCL8 及其mRNA 表达水平增高,并与病情的严重程度相关。CXCL8 参与支原体肺炎的发病过程,并对病情的轻重程度和转归有一定的提示作用。阿奇霉素可通过抑制肺炎支原体增殖途径降低患儿血清中CXCL8 含量、下调CXCL8 mRNA 的表达,逐渐抑制由肺炎支原体介导的免疫损伤。     

Constitutive expression of growth regulated oncogene (<Emphasis Type="Italic">gro</Emphasis>) in human colon carcinoma cells with different metastatic potential and its role in regulating their metastatic phenotype

The purpose of this study was to examine the expression and functional significance of the growth-regulated oncogene (gro) family in human colon carcinoma growth and metastasis. We examined constitutive expression of CXCL1 (gro-α), CXCL2 (gro-β), CXCL3 (gro-γ) and their receptor, CXCR2 in human colon carcinoma cells with different metastatic potentials. Non-metastatic and low metastatic cells expressed lower levels of CXCL1 and CXCR2 mRNA and protein as compared to high metastatic colon carcinoma cells. No difference in CXCL2 and CXCL3 mRNA expression levels was observed. Colon carcinoma cells expressing higher levels of CXCL1 exhibit increased proliferation and invasive potential. Furthermore, exogenous addition of recombinant human CXCL1 significantly enhanced the proliferation and invasiveness of colon carcinoma cells. Furthermore, treatment of KM12C cells with exogenous CXCL1 enhanced their invasiveness. Neutralizing antibody to CXCL1 in combination with antibody to CXCR2 inhibited highly metastatic KM12L4 (high CXCL1 expressor) cell proliferation. These data demonstrate that the constitutive expression of CXCL1 and its receptor CXCR2 is associated with metastatic potential and modulates colon cancer cell proliferation and an invasive phenotype.This revised version was published online in August 2005 with a corrected cover date.     

Glutathione S-Transferase P1 Correlated with Oxidative Stress in Hepatocellular Carcinoma

Background: Glutathione-S-transferase P1 (GSTP1) is an important phase II enzyme that can protect cells from oxidative stress in various human cancers. However, few clinical studies were undertaken on the relationship between GSTP1 and oxidative stress in hepatocellular carcinoma (HCC). The present study was therefore aimed to evaluate the potential associations between GSTP1 and oxidative stress in HCC patients.Methods: The GSTP1 expression in peripheral blood mononuclear cells (PBMCs) was determined by flow cytometry from 38 HCC patients and 38 chronic hepatitis B (CHB) patients. The GSTP1 mRNA level in PBMCs was determined by real-time quantitative polymerase chain reaction. Enzyme-linked-immunosorbent-assay (ELISA) was performed to measure the oxidative stress status, including plasma levels of malondialdehyde (MDA), xanthine oxidase (XOD), reduced glutathione hormone (GSH) and glutathione-S-transferases (GST).Results: Significantly decreased GSTP1 protein expression was found in HCC patients than in CHB patients (P<0.05). The GSTP1 mRNA expression of HCC patients was also decreased compared with CHB patients (P<0.05). MDA and XOD levels were significantly higher in HCC patients than in CHB patients, while plasma GSH and GST levels were statistically lower in HCC patients than in CHB patients. GSTP1 expression level was correlated with plasma levels of MDA (P<0.01), XOD (P = 0.01) and GSH (P< 0.01), GST (P< 0.01).Conclusion: We demonstrated that the reduced GSTP1 expression might contribute to oxidative stress in the development of HCC from CHB.     

CD168 对口腔鳞状细胞癌增殖、 侵袭的作用机制研究

目的 探究 CD168 对口腔鳞状细胞癌增殖、 侵袭的作用机制。 方法 比较人正常口腔角质细胞 系 HOK 与不同口腔鳞癌细胞株间 CD168 表达差异, 选择 HN13 细胞株作为研究对象, 感染慢病毒 shRNA 载体后, 实时荧光定量 PCR (RT-qPCR) 和 Western 印迹法检测 CD168 基因和蛋白表达检测干预效果, CCK-8 法检测细胞增殖情况, 流式细胞仪检测细胞凋亡率, Transwell 试验检测细胞侵袭情况, Western 印迹 检测细胞增殖、 凋亡、 侵袭以及 CXCL12-CXCR4 / CXCR7 信号轴相关蛋白表达。 结果 选择 HN13 细胞和 CD168-shRNA2 慢病毒载体进行后续实验 (P< 0. 05); 沉默 CD168 可使 HN13 细胞增殖、 侵袭数量减少, 细胞凋亡率升高 (P< 0. 05), VEGF、 PCNA、 MMP-2、 MMP-9、 CXCL12、 CXCR4、 CXCR7 蛋白表达量降低 (P< 0. 05), Bax / Bcl-2 比值升高 (P< 0. 05), shRNA-NC 组变化无统计学意义 (P> 0. 05)。 结论 靶向沉 默 CD168 可抑制口腔鳞状癌细胞 HN13 增殖、 侵袭, 促进其凋亡, 可能与 CXCL12-CXCR4 / CXCR7 信号轴 有关。     

Pleiotropic effects of CXC chemokines in gastric carcinoma: differences in CXCL8 and CXCL1 expression between diffuse and intestinal types of gastric carcinoma

CXC chemokines modulate host immunity, neovascularization, growth and invasive behaviour of tumours. Despite their relevance in tumour biology, chemokine expression in intestinal- and diffuse-type gastric carcinoma, which exhibit a completely different growth pattern, has not been investigated in detail. In this study, expression of the CXC chemokines CXCL8 [interleukin (IL)-8], CXCL1 [growth-related oncogene alpha (Gro alpha)], CXCL9 [monokine induced by interferon (IFN)-gamma] and CXCL10 [IFN-gamma-inducible protein-10 (IP-10)] and the corresponding chemokine receptors CXCR1-3 was investigated by immunohistochemistry in intestinal- and diffuse-type gastric carcinoma. Tumour cells of all patients expressed CXCL8. CXCL8 expression was significantly stronger in tumour cells of diffuse- rather than intestinal-type gastric carcinoma (P < 0.01) as determined by a semiquantitative score. CXCL1 was expressed almost exclusively by diffuse- but not intestinal-type carcinoma cells. The corresponding chemokine receptors, CXCR1 and CXCR2, were found on carcinoma cells. Furthermore, CXCL8 expression correlated with number of tumour vessels (P < 0.01), suggesting an angiogenetic function in gastric carcinoma not only in vitro but also in vivo. CXCL10 and CXCL9, attractants for T cells, were expressed by peritumorous macrophages in close proximity to IFN-gamma-producing CXCR3-positive T cells in both tumour types. These chemokines may attract gastric carcinoma-infiltrating T cells via an IFN-gamma-mediated pathway and enhance host immunity against the tumour. In gastric carcinoma a complex interplay between CXC-chemokine signals derived from both tumour cells and tumour-infiltrating immune cells may exhibit pleiotropic effects in tumour biology that go far beyond their originally described functions as leucocyte chemoattractants. Because CXCL8 and CXCL1, which are known to increase growth and invasive behaviour of malignant tumours, are significantly stronger expressed in diffuse- than intestinal-type gastric carcinoma, one may speculate that these chemokines influence the different growth pattern of gastric carcinoma types.     

Roles of Chemokine Receptor 4 （CXCR4） and Chemokine Ligand 12 （CXCL12） in Metastasis of Hepatocellular Carcinoma Cells

Chemokines are involved in human hepatocellular carcinoma （HCC） carcinogenesis. However, the exact mechanism of chemokines in HCC carcinogenesis remains unknown. Here we investigated the roles of chemokine receptor 4 （CXCR4） and chemokine ligand 12 （CXCL12） in the metastasis of HCC. We found that the expression levels of CXCR4 mRNA in HCC tissues, MHCC97 cells, and HUVEC cells were 2.52 ±1.13, 2.34 ±1.16 and 1.63 ±1.26, respectively and that the CXCR4 protein levels were 1.38 ± 0.13, 1.96± 0.32 and 1.86 ±0.21, respectively. In contrast, CXCR4 was not detected in normal hepatic tissues. In 78 HCC patients, we also found that the concentration of CXCL12 in cancerous ascitic fluid was 783-8,364 pg/ml and that CXCL12 mRNA level in HCC metastasis portal lymph nodes was 1.21 ± 0.87 but undetectable in normal hepatic tissues. Finally we discovered that recombinant human CXCL12 could induce MHCC97 cells and HUVEC cells to migrate with chemotactic indexes （CI） of 3.9 ±1.1 and 4.1± 1.6, respectively. Cancerous ascitic fluid could also induce the migration of MHCC97 cells with a CI of 1.9 ± 0.8. Thus, our data suggest that CXCR4 and CXCL12 may play an important role in the metastasis of HCC by promoting the migration of tumor cells.